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Fetal major cardiac defects and placental dysfunction at 11–13 weeks' gestation
Author(s) -
Fantasia I.,
Kasapoglu D.,
Kasapoglu T.,
Syngelaki A.,
Akolekar R.,
Nicolaides K. H.
Publication year - 2018
Publication title -
ultrasound in obstetrics and gynecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.202
H-Index - 141
eISSN - 1469-0705
pISSN - 0960-7692
DOI - 10.1002/uog.18839
Subject(s) - medicine , fetus , gestation , cardiac function curve , perfusion , placental growth factor , placenta , cardiology , ventricular outflow tract , obstetrics , pregnancy , heart failure , vascular endothelial growth factor , genetics , vegf receptors , biology
Objective To investigate the relationship between fetal major cardiac defects and markers of placental perfusion and function. Methods This was a prospective screening study in singleton pregnancies at 11–13 weeks' gestation. Uterine artery pulsatility index (UtA‐PI), serum pregnancy‐associated plasma protein‐A (PAPP‐A) and placental growth factor (PlGF) were measured and the values were converted into multiples of the normal median (MoM). Median MoM values in fetuses with isolated major cardiac defects were compared with those in fetuses without major defects. Results The 50 094 singleton pregnancies fulfilling the entry criteria included 49 898 pregnancies with normal cardiac anatomy and 196 (0.39%) with major congenital cardiac defects: 73 (37.2%) with conotruncal defects, 63 (32.1%) with left ventricular outflow tract defects and 60 (30.6%) with valvular defects. In the group with cardiac defects, compared with controls, there was lower median PAPP‐A MoM (0.81 vs 1.00, P < 0.0001) and PlGF MoM (0.78 vs 1.00, P < 0.0001) but no significant difference in UtA‐PI MoM (1.01 vs 1.00, P = 0.162). Conclusion In pregnancies with isolated fetal major cardiac defects, there is evidence of placental dysfunction in the absence of impaired placental perfusion. Copyright © 2017 ISUOG. Published by John Wiley & Sons Ltd.

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